Sulforaphane as a promising molecule for fighting cancer

被引:195
作者
Fimognari, Carmela [1 ]
Hrelia, Patrizia [1 ]
机构
[1] Univ Bologna, Dept Pharmacol, I-40126 Bologna, Italy
关键词
sulforaphane; cancer; apoptosis; initiation; promotion; progression;
D O I
10.1016/j.mrrev.2006.10.004
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
A number of natural compounds with inhibitory effects on tumorigenesis have been identified from our diet. Several studies have documented the cancer-preventive activity of a significant number of isothiocyanates (ITCs), the majority of which occur in plants, especially in Cruciferous vegetables. The most characterized ITC is sulforaphane (SFN). SFN has received a great deal of attention because of its ability to simultaneously modulate multiple cellular targets involved in cancer development, including: (i) DNA protection by modulating carcinogen-metabolizing enzymes and blocking the action of mutagens; (ii) inhibition of cell proliferation and induction of apoptosis, thereby retarding or eliminating clonal expansion of initiated, transformed, and/or neoplastic cells; (iii) inhibition of neoangiogenesis, progression of benign tumors to malignant tumors, and metastasis fort-nation. SFN is therefore able to prevent, delay, or reverse preneoplastic lesions, as well as to act on cancer cells as a therapeutic agent. Taking into account this evidence and its favorable toxicological profile, SFN can be viewed as a conceptually promising agent in cancer prevention and/or therapy. (C) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:90 / 104
页数:15
相关论文
共 104 条
[1]   Sulforaphane induces inhibition of human umbilical vein endothelial cells proliferation by apoptosis [J].
Asakage M. ;
Tsuno N.H. ;
Kitayama J. ;
Tsuchiya T. ;
Yoneyama S. ;
Yamada J. ;
Okaji Y. ;
Kaisaki S. ;
Osada T. ;
Takahashi K. ;
Nagawa H. .
Angiogenesis, 2006, 9 (2) :83-91
[2]   Sulforaphane and quercetin modulate PhIP-DNA adduct formation in human HepG2 cells and hepatocytes [J].
Bacon, JR ;
Williamson, G ;
Garner, RC ;
Lappin, G ;
Langouët, S ;
Bao, YP .
CARCINOGENESIS, 2003, 24 (12) :1903-1911
[3]   Production of DNA strand breaks by N-nitrosodimethylamine and 2-amino-3-methylimidazo[4,5-f]quinoline in THLE cells expressing human CYP isoenzymes and inhibition by sulforaphane [J].
Barceló, S ;
Macé, K ;
Pfeifer, AMA ;
Chipman, JK .
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 1998, 402 (1-2) :111-120
[4]   CYP2E1-mediated mechanism of anti-genotoxicity of the broccoli constituent sulforaphane [J].
Barcelo, S ;
Gardiner, JM ;
Gescher, A ;
Chipman, JK .
CARCINOGENESIS, 1996, 17 (02) :277-282
[5]   Sulforaphane and its glutathione conjugate but not sulforaphane nitrile induce UDP-glucuronosyl transferase (UGT1A1) and glutathione transferase (GSTA1) in cultured cells [J].
Basten, GP ;
Bao, YP ;
Williamson, G .
CARCINOGENESIS, 2002, 23 (08) :1399-1404
[6]   Inhibition of angiogenesis and endothelial cell functions are novel sulforaphane-mediated mechanisms in chemoprevention [J].
Bertl, E ;
Bartsch, H ;
Gerhäuser, C .
MOLECULAR CANCER THERAPEUTICS, 2006, 5 (03) :575-585
[7]  
Bonnesen C, 2001, CANCER RES, V61, P6120
[8]  
Brooks JD, 2001, CANCER EPIDEM BIOMAR, V10, P949
[9]   Active cell death induced by the anti-estrogens tamoxifen and ICI 164 384 in human mammary carcinoma cells (MCF-7) in culture: The role of autophagy [J].
Bursch, W ;
Ellinger, A ;
Kienzl, H ;
Torok, L ;
Pandey, S ;
Sikorska, M ;
Walker, R ;
Hermann, RS .
CARCINOGENESIS, 1996, 17 (08) :1595-1607
[10]   Angiogenesis in cancer and other diseases [J].
Carmeliet, P ;
Jain, RK .
NATURE, 2000, 407 (6801) :249-257